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Cited by 73

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

Disabled-2 Is an Epithelial Surface Positioning Gene

Yang, Dong-Hua, Cai, Kathy Q., Roland, Isabelle H., Smith, Elizabeth R., Xu, Xiang-Xi·2007·Journal of Biological Chemistry
DOI 10.1074/jbc.m611356200
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Crossref · 10.1074/jbc.m611356200

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4 of 4 references verified0 citation errors · 0 not checkable

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  • Dab2's functions in mediating polarized trafficking of cell adhesion molecules such as integrins and E-cadherin provide possible mechanisms for failure in endoderm epithelial polarity, sorting, and organization of Dab2 deleted embryos.

    “Thus, its functions in mediating polarized trafficking of cell adhesion molecules such as integrins and E-cadherin provide possible mechanisms for failure in endoderm epithelial polarity, sorting, and organization of Dab2 deleted embryos”

    From Endocytosis and Physiology: Insights from Disabled-2 Deficient Mice (2016) · cites this paper as Yang et al., 2007

    The Discussion and Figure 6 describe Dab2-dependent E-cadherin trafficking as a proposed mechanism for epithelial polarity and surface positioning; the figure links loss of polarity to disorganization of Dab2-deficient endoderm cells. The paper mentions integrins as adhesion molecules, but the passages do not establish Dab2-mediated polarized trafficking of integrins. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Dab2 participates in clathrin-mediated endocytosis and trafficking of E-cadherin, explaining its effects on epithelial organization.

    “Also, participation in the clathrin-mediated endocytosis and trafficking of E-cadherin explains its affects on epithelial organization (Yang et al., 2007).”

    From Endocytosis and Physiology: Insights from Disabled-2 Deficient Mice (2016) · cites this paper as Yang et al., 2007

    The Discussion says Dab2 is important for E-cadherin distribution and suggests that Dab2-mediated clathrin-coated endocytosis removes E-cadherin from the apical surface. The Abstract proposes loss of polarity as the mechanism behind defective epithelial surface positioning. The citing sentence presents that proposed explanation as established. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

  • Conventional dab2 gene deletion in mice results in early embryonic death.

    “Conventional dab2 gene deletion in mice results in early embryonic death”

    From Endocytic adaptors Arh and Dab2 control homeostasis of circulatory cholesterol (2016) · cites this paper as [28]

  • Dab2 functions in endocytic trafficking to sustain cell polarity and epithelial organization; loss of Dab2 leads to endoderm epithelial disorganization and embryonic failure.

    “Therefore, Dab2 functions in endocytic trafficking to sustain cell polarity and thus epithelial organization, and hence loss of Dab2 leads to endoderm epithelial disorganization and failure of the embryos”

    From Endocytosis and Physiology: Insights from Disabled-2 Deficient Mice (2016) · cites this paper as Yang et al., 2007

  • Dab2 tumor suppressor function is attributed to epithelial organization.

    “epithelial organization (Sheng et al., 2000b; Yang et al., 2002b, 2007)”

    From Endocytosis and Physiology: Insights from Disabled-2 Deficient Mice (2016) · cites this paper as Yang et al., 2007

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Citations

Cites

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Research works printed but not linked: 47

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Metadata

Authors
Yang, D.-H., Cai, K. Q., Roland, I. H., Smith, E. R., & Xu, X.-X.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2007-04
Volume
282
Issue
17
Pages
13114-13122
ISSN
0021-9258
DOI
10.1074/jbc.m611356200
Cited by
73
References
4
Language
en
Licence

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